Changes induced by sucrose administration upon the morphology and function of pancreatic islets in the normal hamster.

Abstract

This report documents sequential changes in islet morphology (cell replication and islet neogenesis) and glucose-induced insulin secretion in young normal male Syrian hamsters. Three-week-old animals received a control standard commercial diet or this diet supplemented with sucrose--10% (w/v) solution in drinking water, a treatment that stimulated pancreatic growth and function--for 5 (C5/S5) or 21 (C21/S21) weeks. Insulin secretion and content were measured in isolated islets, while several biochemical parameters were assessed in serum. Different morphological features were analysed in the endocrine pancreas by quantitative immunocytochemistry. Serum glucose, triglycerides and total cholesterol levels were comparable among the groups, whereas serum- and pancreatic-insulin levels were higher in the S hamsters. Islets from S21 hamsters released more insulin than those from C21 animals at all glucose concentrations tested. The volume densities of the total endocrine pancreas (1.9 +/- 0.2 vs 1.2 +/- 0.2; p < 0.02) of the beta-cell subpopulation, the islet number per unit area (2.4 +/- 0.1 vs 1.2 +/- 0.1; p < 0.0004) and the beta-cell mass (4.2 +/- 0.5 vs 2.3 +/- 0.5; p < 0.01) were significantly higher in S5 vs C5 animals. Conversely, the islet volume and the number of beta cells/islets were significantly smaller in S5 than in C5 animals. The beta-cell replication rate in S5 hamsters was 10-fold that of C5 animals. All these parameters had comparable values in S21 and C21 animals. We detected cytokeratin-labelled cells located at the islet periphery (in alpha cells) and among the ductular cells, only in the S5 hamsters. Sucrose administration to young hamsters causes time-dependent pancreatic modifications, with morphological changes (increase in islet- and in beta-cell mass with incremented beta-cell replication rate and evidence of islet neogenesis) occurring at 5 weeks and insulin secretion (increase in insulin sensitivity to glucose) being mainly affected at 21 weeks. This experimental model could prove useful for studying the mechanisms underlying the control of islet-cell population distribution and for developing new strategies in preventing cell damage.